Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or 57 [75% for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo-and nifedipine-treated patients (16.9 + 1.5 MB-CK-geq/m ,n 65, and 17.0 ± 1l.5 MB-CK-geq/m', n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10. 1 % for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .0 18). There were no significant differences in 2 week and 6 month mortalities in the group of all participating patients, which included 10 patients randomly assigned therapy but retrospectively determined to be ineligible. Two week mortality for this group (n = 181) was 2.3% for placebo-and 7.5% for nifedipine-treated patients and 6 month mortality was 11.4% for placebo-and 10.8% for nifedipine-treated patients. Thus, nifedipine therapy did not prevent progression of threatened myocardial infarction to the acute event or limit infarct size in patients who experienced infarction. There was a statistically significant increase in 2 week mortality with nifedipine in the group of eligible patients randomly assigned to a regimen, but mortality was balanced when results were analyzed for all patients taking part in the randomization protocol.

No abstract

To characterize the potential of nifedipine in the therapy of unstable angina pectoris we implemented a blinded, randomly assigned, titrated schedule of conventional therapy (propranolol, if not contraindicated, and isosorbide dinitrate) or nifedipine for 14 days in 126 patients hospitalized in a coronary care unit for ischemic chest pain of less than 45 min duration. There were no significant differences between conventionally and nifedipine-treated patients with regard to (1) the time to relief of pain as judged by life table analysis, (2) the decrease in anginal attacks per 24 hr from day 0 to day 2 ( -2.5 + 0.4 for conventional therapy vs; -2.8 + 0.3 for nifedipine), (3) the decrease in the number of nitroglycerin tablets consumed per 24 hr ( -2.0 ± 0.5 for conventional vs -2.1 ± 0.4 for nifedipine therapy), (4) the percentage of patients requiring morphine on day 1 (1 3% for conventional vs 21 % for nifedipine therapy), or (5) the percentage of patients who developed infarction (1 4% in both groups). Among the 27 patients who did not respond to initial conventional (n = 13) or nifedipine therapy (n = 14), five in each group became pain free when the opposite therapy (either nifedipine or conventional therapy) was added. In the subgroup of 67 patients who were receiving propranolol before randomization, addition of nifedipine was more effective in controlling pain than was an increase in conventional therapy (p = .026). In the subgroup of 59 patients not receiving prior propranolol, initiation of conventional therapy produced more rapid pain relief than initiation of nifedipine therapy alone (p < .001), which tended to increase heart rate. Thus, for the study population as a whole therapy with nifedipine alone was equivalent to conventional therapy for unstable angina, although this overall equivalence may result from a combination of superiority of nifedipine therapy in patients previously receiving ,/-blocker therapy and superiority of /3-blocker therapy in patients not previously receiving ,3-blockers. Circulation 69, No. 4, 728-739, 1984. UNSTABLE ANGINA, a syndrome intermediate in severity between stable angina pectoris and acute myocardial infarction, is well recognized. Heberden,' in his classic description of angina pectoris, noted that in some cases the pain occurred in patients at rest. Her-